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Circulation, Vol 84, 1235-1245, Copyright © 1991 by American Heart Association

ARTICLES

Transmural distribution of myocardial tissue growth induced by volume- overload hypertrophy in the dog

JH Omens and JW Covell
Department of Medicine, University of California San Diego, La Jolla 92093-0613.

BACKGROUND. Although chronic volume overload is thought to induce uniform cardiac enlargement, the stimulus for tissue growth has not been defined. Changes in diastolic and systolic stress or strain have been proposed as mechanical factors that may stimulate hypertrophy. Since there are thought to be transmural variations in these stresses and strains, three-dimensional patterns of myocardial tissue growth may provide insight into the role of these factors. METHODS AND RESULTS. To assess the transmural variation in tissue growth after volume overload, the configurations of three columns of four to six gold beads (1-mm diameter) implanted in the left ventricular anterior free wall were recorded in five dogs before and after cardiac enlargement induced by creating a systemic arteriovenous fistula. Data were obtained with end- diastolic pressures adjusted to the same level in the control and hypertrophic states. End-diastolic wall thickness remained constant, whereas left ventricular diameter increased. Small increases in transmural systolic strain were seen. The volumes defined by four beads (a tetrahedron) at end diastole showed increases in myocardial mass of 20-27% after 3.6 (mean) weeks of hypertrophy and were uniform across the wall of the left ventricle. The edges of single bilinear-quadratic finite elements were fitted to the three columns of the bead set at end diastole in control and at end diastole after hypertrophy at equal end- diastolic pressures. Thus, continuous transmural strain distribution were obtained at the hypertrophic state with respect to the control state. The transmural distributions of these end-diastolic growth strains were uniform and positive for both the circumferential and longitudinal components measured in a cardiac coordinate system, with small radial growth strain indicating that growth was predominantly parallel to the epicardial tangent plane. Moreover, when strains were transformed (rotated) to fiber coordinates, in-plane fiber and cross- fiber growth strains were both positive at all locations across the wall and approximately equal in magnitude, indicating considerable growth in the cross-fiber direction. CONCLUSIONS. These results indicate that the stimulus for volume-overload hypertrophy may be constant across the wall and that substantial cross-fiber growth occurs during volume-overload hypertrophy.

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